This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We continue investigating functions of apolipoprotein L1 (ApoL1) and ApoL2 in the induction of autophagy, a self-eating mechanism, in cancer cell death. Autophagy is normally used by cells to recycle the building blocks, such as amino acids, nucleic acids and fatty acids, for resynthesize macromolecules, such as proteins, DNA and RNA and lipids. Recent study also showed that autophagy can function as a programmed cell death mechanism to eliminate damaged cells. Our recent results showed that ApoL1 is one of the molecular regulators that induces autophagic cell death in various cancer cell types and its closely related protein ApoL2 can synergistically enhance ApoL1-induced cell death. Both ApoL1 and L2 are potential biomarkers for diagnosis, prognosis and treatment of human cancers.